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part 2c > Hypertension > Flashcards

Hypertension Flashcards

1
Q

what is hypertension?

A

High blood pressure

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2
Q

what is ventricular hypertrophy?

A

heart muscles becomes enlarged and thickened

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3
Q

Causes of hypertension:

What does primary hypertension mean?

A

HBP with no apparent individual cause

‘assymptomatic’

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4
Q

Causes of hypertension:

What is secondary hypertension

A
  • when the cause is known
    e. g
  • adrenal gland disorders
  • kidney diseases - tumor, failures
  • drugs - anti- inflammatory corticosteroids - prednisone , birth control, cold medicines
  • pregnancy
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5
Q

What is the normal BP?

A

120/80

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6
Q

BP : 120/80

what is the systolic BP and diastolic BP

A

1st is systolic BP

2nd is diastolic BP

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7
Q

what is clinic BP?

A

> 140/90

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8
Q

What are the classifications of hypertension

A
  • clinical BP

- ABPM( ambulatory blood pressure measurements) and HBPM (home blood pressure measurements)

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9
Q

what is the difference between ABPM and HBPM?

A

ABPM: during one 24-hour period, whereas
HBPM : assesses blood pressure at specific times during the day and night over a longer period of time while the patient is seated and resting.

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10
Q

what is the treatment strategy for hypertension (nice guidelines)

A

hypertension with type 2 diabetes or without 2 type but aged 55 or younger and not black/ african Caribbean

  • 1 ) ACEi or ARB
    2) ACEi or ARB and CCB/thiazide like diuretics
    3) ACEi or ARB and CCB and thiazide like diuretics
    4) seek expert advice

Hypertension for patients aged 55 or older and black/ african Caribbean

1) CCB
2) CCB + ACEi or ARB or thiazide like diuretics
3) ACEi or ARB and CCB and thiazide like diuretics
4) seek expert advice

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11
Q

what are the regulation factors of blood pressure?

A
  • blood volume
  • blood viscosity
  • cardiac output
  • total peripheral resistance
  • BP - CO * TPR
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12
Q

what are resistance vessels?

A
  • small arteries and arterioles
  • largest pressure drop occurs here
  • thus contractile state of these arteries has a massive impact on blood pressure
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13
Q

BP is regulated by which reflex?

A
  • aortic baroreceptor

- send small signals to the brain which controls the vasculature in the heart

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14
Q

How to maintain a normal blood pressure

- stimulus high blood pressure

A
  • stimulus - high blood pressure
  • arterial blood pressure is higher than normal range
  • stimulation of baroreceptors which is located in the aortic arch and carotid sinus
  • this causes the stimulation of cardio-inhibitory centre
  • inhibits the vasomotor centre
  • reaches the brain
  • reaches the heart
  • decrease in sympathetic impulses which causes decrease in heart rate and decrease in contractility
  • which causes decrease in cardiac output
  • decrease vasomotor impulses which allows vasodilation - the vessel diameter increases
  • this causes peripheral resistance to decrease
  • as peripheral resistance and cardiac output decreases it will cause the BP to return to a homeostatic range
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15
Q

How to maintain a normal blood pressure?

-when the bp is low

A
  • stimulus - low blood pressure
  • arterial blood pressure is lower than normal range
  • inhibition of baroreceptors which is located in the aortic arch and carotid sinus
  • this causes the inhibit of cardio-inhibitory centre and stimulate cardio- accelerating centre
  • stimulate the vasomotor centre
  • reaches the brain
  • reaches the heart
  • increase in sympathetic impulses which causes increase in heart rate and increase in contractility
  • which causes increase in cardiac output
  • vasomotor fibres stimulate vasoconstriction
  • this causes peripheral resistance to increase
  • as peripheral resistance and cardiac output increases it will cause the BP to return to a homeostatic range
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16
Q

Explain contraction of smooth muscles cells?

A

thick filaments contain myosin
thin filaments contain actin
when these muscle cells contract
they slide across each other
and shorten the length of the smooth muscle cells
when this happens around a lumen - smooth muscle cells slide across each other and the lumen contracts when this happens and dilate when they relax

17
Q

Explain vascular smooth muscle contraction

A
  1. Starts of with GPCR
    1. An agonist binds to the G alpha q receptor (noradrenaline) which is released from sympathetic nerves
    2. Releases of PIP2 and PLC (phospholipase C)
    3. This releases the production of DAG (diglycerol) and IP3 (inositol trisphosphate)
    4. IP3 binds to receptors on the sarcoplasmic reticulum (SR) within the smooth muscle cell
    5. This releases calcium from the intracellular store
    6. Calcium which is released binds to a signalling molecule called calmodulin
    7. Calcium release causes the plasma membrane to depolarise - more positive charge within the cytoplasm
    8. Voltage gated calcium channels sends the depolarisation which activates the channels
    9. Calcium enters the cells along its concentration gradient
    10. These calcium will also bind to the calmodulin molecules - calcium induced starting signals
    11. Calmodulin activates MCLK ( Myosin light chain kinase)
    12. This enzyme phosphates and adds a phosphate group to the myosin light chain (MLC)
    13. Which causes constriction - due to the phosphorylation of MCLK
18
Q

when the calcium increases in the endothelial cell layer what happens to the calcium level in the smooth muscle cell layer.

A

it will decrease and cause relaxation

19
Q

endothelium-dependent relaxation - nitric oxide

A

increase in EC (ca2+) activate nitric oxide synthase
nitric acid diffuses to smooth muscle cells and activates soluble guanylate cyclase( sGC) generating cGMP
cGMP causes relaxation by activating protein kinase G (PKG)
PKG prevents ca2+ release and ca2+ entry also evoke MLCK to evoke relaxation

20
Q

what is the function of vasodilator drugs?

A
  • relaxes smooth muscles
    e. g
  • nitrates generate NO
  • potassium channel activators hyperpolarize smooth muscles preventing calcium entry via VGCC
  • CCB directly inhibit VGCC
  • some vasodilators do not relax smooth muscles directly
  • prevent the action of vasoconstrictors such as noradrenaline or angiotensin
21
Q

what are calcium channel blockers and their mechanism

A
  • block CCVG on the smooth muscle cells
  • prevent calcium entering
  • Block calmodulin
  • Block myosin light chain kinase
  • Block the phosphorylation
  • Block constriction
  • Reduction in total peripheral resistance
  • Reduction in blood pressure
22
Q

Block L- Type VGCC have 3 categories what are they?

A

dihydropyridines - nifedipine amlopipine - felodipine - lacidipine
phenethylakylamine - verapamil
benzothiazepine - diltaizam

23
Q

what are the side effects of CCB

A
  • ankle swelling
  • tremor
  • constipation
  • hypotension
  • cardiac effect - AV block, weakened heart beat
24
Q

what is the mechanism of action of potassium channel activators

A
  • agonist binds
  • calcium enters via VGCC
    calcium binds to calmodulin
    activates myosin light kinase
    which gets phosphorylated
    this causes constriction
  • Potassium levels inside cells is much higher than outside cells
  • When potassium channels open the positive k will leave the cell and flow down concentration gradient to outside the cell
  • Lead to a loss of positive charge from within the cell
  • Eventually Causes ( when a lot of potassium channels are open) hyperpolarisation or movement to more negative membrane potentials within the cytoplasm of the cell
  • Which will lead to the closure of the vgcc
  • And once they close the whole process of constriction is blocked
  • Relax the smooth muscle cells and arteries
  • Reduce total peripheral resistance
    Blood pressure decreases
25
Q

what is atria-ventricular block- how is it caused

A

Block the conduction of the heart beat between the atria and the ventricles - l type vgcc contributes in the pacemaker activity which allows the conduction

26
Q

how does the heart beat get weak in relation to ccb?

A

Blocking l type vgcc will reduce the strength of contraction of the heart

27
Q

what is cardiac ouput

A

work performed by the heart

28
Q

what is total pheripheral resistance

A

resistance to blood flow

29
Q

explain Reflex tachycardia - side effect of pca

A
  • Drop in bp
    • Baroreceptor reflex - going to sense by the body
    • Tell cardiovascular centre in the brain that bp is dropped
    • When bp is dropped the body wants to increase the total peripheral resistance and cardiac output inorder to restore the bp
    • When pcb is used - effective on vaculature to reducr tpr but do not have much effect on the heart
      When baroreceptor reflex is triggered - tpr remains low but co increases- increases the heart rate = reflex tachycardia
30
Q

examples of alpha 1 adrenoreceptor antaginist and what they do and what are their side effects

A

prazosin
doxazosin
urapidil

block action of sympthetic nervous system on resistance arteries - vasolidation - decrease in bp

side effects
- reflex tachycardia
fattigue
dizziness

31
Q

what is postural hypotension:

A

rapidly getting up from lying to standing, feel dizzy,

  • lying down its much easier for the blood to reach the brain
  • when you stand up all the blood is drained from the upper part
  • dizzy until blood vessels in the lower part of the body contract
  • contraction restores blood flow back up to the head
32
Q

what are examples of CCB

A 
verapamil 
diltaizam 
amlodipine 
nifedipine 
lacidipine 
felopine
33
Q

what are examples of PCA

A
  • minoxidil

- diaoxide

part 2c (18 decks)

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